Failure of medial forebrain bundle or raphe ablation to alter the daily temperature rhythm of the rat.

The data presented in the present study suggest that neither the ascending noradrenergic fibres confined to the MFB nor the serotonergic fibres originating in or passing through the mesencephalic raphe are essential for periodicity in body temperature. Both control and experimental groups, i.e., rats subjected to medial forebrain bundle or raphe ablation presented circadian periodicity in body temperature and neither the phase, amplitude or overall mean of experimentals differed significantly from controls.     

Role of lactone ring of aflatoxin B1 in toxicity and mutagenicity

Cleavage of the lactone ring of aflatoxin B1 results in a nonfluorescent compound that has greatly reduced biological activity. Mutagenicity, as measured by the Ames test, is reduced 450-fold compared to that of B1, and toxicity, as measured by the chick embryo test, is reduced 18-fold.     

Role of lactone ring of aflatoxin B1 in toxicity and mutagenicity

Summary Cleavage of the lactone ring of aflatoxin B₁ results in a nonfluorescent compound that has greatly reduced biological activity. Mutagenicity, as measured by the Ames test, is reduced 450-fold compared to that of B₁, and toxicity, as measured by the chick embryo test, is reduced 18-fold.     

Immunization with amyloid-beta attenuates Alzheimer-disease-like pathology in the PDAPP mouse.

Amyloid-beta peptide (Abeta) seems to have a central role in the neuropathology of Alzheimer's disease (AD). Familial forms of the disease have been linked to mutations in the amyloid precursor protein (APP) and the presenilin genes. Disease-linked mutations in these genes result in increased production of the 42-amino-acid form of the peptide (Abeta42), which is the predominant form found in the amyloid plaques of Alzheimer's disease. The PDAPP transgenic mouse, which overexpresses mutant human APP (in which the amino acid at position 717 is phenylalanine instead of the normal valine), progressively develops many of the neuropathological hallmarks of Alzheimer's disease in an age- and brain-region-dependent manner. In the present study, transgenic animals were immunized with Abeta42, either before the onset of AD-type neuropathologies (at 6 weeks of age) or at an older age (11 months), when amyloid-beta deposition and several of the subsequent neuropathological changes were well established. We report that immunization of the young animals essentially prevented the development of beta-amyloid-plaque formation, neuritic dystrophy and astrogliosis. Treatment of the older animals also markedly reduced the extent and progression of these AD-like neuropathologies. Our results raise the possibility that immunization with amyloid-beta may be effective in preventing and treating Alzheimer's disease.     

高斯杂波中距离扩展目标的模糊CFAR检测

为提高高分辨雷达的检测性能,提出了一种高斯杂波背景下距离扩展目标的模糊检测方法。该方法采用模糊恒虚警率(constant false alarm rate, CFAR)检测器代替传统的二进制CFAR检测器,将距离单元值转换成映射到虚警空间的模糊隶属函数值,然后采用模糊积累准则进行积累,得到检测统计量。研究了模糊代数积、模糊代数和两种积累准则,推导出这两种方法虚警概率的数学解析式。仿真结果表明,高斯杂波背景下模糊代数积积累较双门限二进制积累可获得近2 dB的性能改善。同时,模糊检测方法只采用单个检测门限,具有易于调节的优点。     

Improved estimates of upper-ocean warming and multi-decadal sea-level rise

Changes in the climate system's energy budget are predominantly revealed in ocean temperatures and the associated thermal expansion contribution to sea-level rise. Climate models, however, do not reproduce the large decadal variability in globally averaged ocean heat content inferred from the sparse observational database, even when volcanic and other variable climate forcings are included. The sum of the observed contributions has also not adequately explained the overall multi-decadal rise. Here we report improved estimates of near-global ocean heat content and thermal expansion for the upper 300 m and 700 m of the ocean for 1950-2003, using statistical techniques that allow for sparse data coverage and applying recent corrections to reduce systematic biases in the most common ocean temperature observations. Our ocean warming and thermal expansion trends for 1961-2003 are about 50 per cent larger than earlier estimates but about 40 per cent smaller for 1993-2003, which is consistent with the recognition that previously estimated rates for the 1990s had a positive bias as a result of instrumental errors. On average, the decadal variability of the climate models with volcanic forcing now agrees approximately with the observations, but the modelled multi-decadal trends are smaller than observed. We add our observational estimate of upper-ocean thermal expansion to other contributions to sea-level rise and find that the sum of contributions from 1961 to 2003 is about 1.5 +/- 0.4 mm yr(-1), in good agreement with our updated estimate of near-global mean sea-level rise (using techniques established in earlier studies) of 1.6 +/- 0.2 mm yr(-1).