Stimulated Amplification of Propagating Spin Waves.

Spin-wave amplification techniques are key to the realization of magnon-based computing concepts. We introduce a novel mechanism to amplify spin waves in magnonic nanostructures. Using the technique of rapid cooling, we create a nonequilibrium state in excess of high-energy magnons and demonstrate the stimulated amplification of an externally seeded, propagating spin wave. Using an extended kinetic model, we qualitatively show that the amplification is mediated by an effective energy flux of high energy magnons into the low energy propagating mode, driven by a nonequilibrium magnon distribution.

Insurance reimbursement for risk-reducing mastectomy and oophorectomy in women with BRCA1 or BRCA2 mutations.

PURPOSE: Risk-reducing surgery is an important option for women with BRCA1 and BRCA2 mutations. There are reports in the literature that insurance reimbursement for these procedures varies greatly. Because health insurance coverage significantly affects medical decision-making, current information regarding reimbursement practices of third-party payers is needed. METHODS: Retrospective study of hospital billing records of 38 women with documented BRCA1 or BRCA2 mutations who underwent either a risk-reducing mastectomy or a risk-reducing oophorectomy between March 1, 1997, and July 30, 2000. RESULTS: Complete billing and reimbursement information was available for 35 women undergoing a total of 39 risk-reducing surgeries. A total of 38 of 39 (97%) risk-reducing surgeries were covered in full, less applicable coinsurance and deductibles. The rate of insurance reimbursement did not vary with type of insurance, personal history of cancer, or type of procedure. CONCLUSION: Insurance carriers reimbursed the vast majority of BRCA mutation carriers undergoing risk-reducing surgery.

Effects of antipsychotic treatment on membrane phospholipid metabolism in schizophrenia.

Several studies have shown an increased membrane phospholipid turnover in brain and blood cells of schizophrenic patients. However the specificity of these findings for schizophrenia and the effects of longterm antipsychotic treatment had yet to be demonstrated. In the present study we measured the concentrations of phospholipids in platelet membranes from 67 neuroleptic-free schizophrenic patients compared to both healthy and psychiatric controls, followed by repeated measurements during a 6 months antipsychotic treatment period. At baseline, levels of the main phospholipid components phosphatidylcholine (PC) and phosphatidylethanolamine (PE) were decreased and lysophosphatidylcholine (LPC), a major breakdown product of phospholipid metabolism, was increased in schizophrenic patients compared to healthy and to psychiatric controls, suggesting a specificity of the findings for schizophrenia. During the first 3-weeks on antipsychotic drug treatment LPC levels decreased to control values, but increased again during the following 6 months, reaching significantly higher levels than controls at the end of this period. Thus, at least in peripheral cells an increased breakdown of phospholipids in schizophrenia appears to be present during the acute episode, being influenced only by initial antipsychotic treatment, but without evidence of a long lasting treatment effect on membrane metabolism.

Immunobiochemical characterization of the NMDA-receptor subunit NR1 in the developing and adult rat brain.

To investigate the developmental and regional expression of the NR1-subunit of the NMDA-receptor on the protein level, two polyclonal antisera [NR1(N) and NR1(C)] were raised against fusion proteins derived from the N- and C-terminal domain of the NR1-subunit, respectively. In Western blots of rat brain membranes, both antisera specifically recognized a single protein band with an apparent molecular size of 115 kDa. The regional distribution of the NR1-subunit immunoreactivity was analyzed in the developing and adult rat brain using sections blotted onto nitrocellulose membranes for immunostaining. With the NR1(N)-antiserum, strongest signals were detected in hippocampus, followed by cortex, striatum and thalamus, and weaker staining was observed in tectum, brainstem and cerebellum of adult brain. The NR1(C)-immunoreactivity exhibited a similar distribution, except that the staining in thalamus, tectum, brainstem and cerebellum was faint or virtually absent. The distinct pattern of NR1(N)- and NR1(C)-immunoreactivity arose during postnatal development. At birth, moderate staining with both NR1-subunit antisera was observed throughout the brain increasing strongly in most brain regions until postnatal day 21. In some brain areas, however, the NR1(C)-, in contrast to the NR1(N)-staining, decreased postnatally e.g. in thalamus, tectum and brainstem. The restricted staining intensity of the NR1(C)-antiserum in particular areas of adult and developing brain appears to reflect the emergence of C-terminal splice variants of the NR1-subunit which are not recognized by the NR1(C)-antiserum.