Research Notes : Four additional lines showing nonfluorescent roots

Fluorescence in soybean roots was first described by Chmelar (1934) and by Chmelar and Mostovoj (1934). Reports of nonfluorescing root phenotypes in both Glycine max and G. soja have been made by Grabe (1957), Fehr and Giese (1971) and Broich (1978). Genetics studies by Delannay and Palmer (1982) indicate that absence of root fluorescence in G. max is controlled by four independent genes; three of these genes are recessive (fr1, fr2 and fr4) and one is dominant (Fr3)

Research Notes : United States : Linkage group 12

Weiss (1970a, b, c, d, e) described linkage groups 1 to 7 in soybean. Buzzell (1974, 1979) and Palmer (1977, 1984) have characterized further link-age group 1. Linkage group 8 was reported by Buzzell et al. (1977) and described further by Palmer and Kaul (1983), Sadanaga (1983) and Sadanaga and Grindeland (1984)

A low power clock generator with adaptive inter-phase charge balancing for variability compensation in 40-nm CMOS

Power dissipation besides chip area is still one main optimization issue in high performance CMOS design. Regarding high throughput building blocks for digital signal processing architectures which are optimized down to the physical level a complementary two-phase clocking scheme (CTPC) is often advantageous concerning ATE-efficiency. The clock system dissipates a significant part of overall power up to more than 50% in some applications. <br><br> One efficient power saving strategy for CTPC signal generation is the charge balancing technique. To achieve high efficiency with this approach a careful optimization of timing relations within the control is inevitable. <br><br> However, as in modern CMOS processes device variations increase, timing relations between sensitive control signals can be affected seriously. In order to compensate for the influence of global and local variations in this work, an adaptive control system for charge balancing in a CTPC generator is presented. An adjustment for the degree of charge recycling is performed in each clock cycle. In the case of insufficient recycling the delay elements which define duration and timing position of the recycling pulse are corrected by switchable timing units. <br><br> In a benchmark with the conventional clock generation system, a power reduction gain of up to 24.7% could be achieved. This means saving in power of more than 12% for a complete number-crunching building block

Research notes: Soybean linkage tests

F2 linkage results are presented in Table 1 with a=XY, b=Xy, c=xY and d = xy for the gene pairs 1 i sted in the form of Xx and Yy. Percentage recombination was obtained from the ratio of products following the method of Inmer and Henderson (1943). Results from testing F3 seeds and seedlings to determine F2 phenotypes indicate possible linkage between seed coat peroxidase (ep) and root fluorescence (fr)

Pathological regional blood flow in opiate-dependent patients during withdrawal: A HMPAO-SPECT study

The aims of the present study were to investigate regional cerebral blood flow (rCBF) in heroin-dependent patients during withdrawal and to assess the relation between these changes and duration of heroin consumption and withdrawal data. The rCBF was measured using brain SPECT with Tc-99m-HMPAO in 16 heroin-dependent patients during heroin withdrawal. Thirteen patients received levomethadone at the time of the SPECT scans. The images were analyzed both visually and quantitatively, a total of 21 hypoperfused brain regions were observed in 11 of the 16 patients. The temporal lobes were the most affected area, hypoperfusions of the right and left temporal lobe were observed in 5 and 5 patients, respectively. Three of the patients had a hypoperfusion of the right frontal lobe, 2 patients showed perfusion defects in the left frontal lobe, right parietal lobe and left parietal lobe. The results of the quantitative assessments of the rCBF were consistent with the results of the qualitative findings. The stepwise regression analysis showed a significant positive correlation (r = 0.54) between the dose of levomethadone at the time of the SPECT scan and the rCBF of the right parietal lobe. Other significant correlations between clinical data and rCBF were not found. The present results suggest brain perfusion abnormalities during heroin withdrawal in heroin-dependent patients, which are not due to the conditions of withdrawal

Bilateral effects of unilateral cerebellar lesions as detected by voxel based morphometry and diffusion imaging

Over the last decades, the importance of cerebellar processing for cortical functions has been acknowledged and consensus was reached on the strict functional and structural cortico-cerebellar interrelations. From an anatomical point of view strictly contralateral interconnections link the cerebellum to the cerebral cortex mainly through the middle and superior cerebellar peduncle. Diffusion MRI (dMRI) based tractography has already been applied to address cortico-cerebellar-cortical loops in healthy subjects and to detect diffusivity alteration patterns in patients with neurodegenerative pathologies of the cerebellum. In the present study we used dMRI-based tractography to determine the degree and pattern of pathological changes of cerebellar white matter microstructure in patients with focal cerebellar lesions. Diffusion imaging and high-resolution volumes were obtained in patients with left cerebellar lesions and in normal controls. Middle cerebellar peduncles and superior cerebellar peduncles were reconstructed by multi fiber diffusion tractography. From each tract, measures of microscopic damage were assessed, and despite the presence of unilateral lesions, bilateral diffusivity differences in white matter tracts were found comparing patients with normal controls. Consistently, bilateral alterations were also evidenced in specific brain regions linked to the cerebellum and involved in higher-level functions. This could be in line with the evidence that in the presence of unilateral cerebellar lesions, different cognitive functions can be affected and they are not strictly linked to the side of the cerebellar lesion

Blood-based biomarkers for Alzheimer disease: mapping the road to the clinic.

Biomarker discovery and development for clinical research, diagnostics and therapy monitoring in clinical trials have advanced rapidly in key areas of medicine - most notably, oncology and cardiovascular diseases - allowing rapid early detection and supporting the evolution of biomarker-guided, precision-medicine-based targeted therapies. In Alzheimer disease (AD), breakthroughs in biomarker identification and validation include cerebrospinal fluid and PET markers of amyloid-β and tau proteins, which are highly accurate in detecting the presence of AD-associated pathophysiological and neuropathological changes. However, the high cost, insufficient accessibility and/or invasiveness of these assays limit their use as viable first-line tools for detecting patterns of pathophysiology. Therefore, a multistage, tiered approach is needed, prioritizing development of an initial screen to exclude from these tests the high numbers of people with cognitive deficits who do not demonstrate evidence of underlying AD pathophysiology. This Review summarizes the efforts of an international working group that aimed to survey the current landscape of blood-based AD biomarkers and outlines operational steps for an effective academic-industry co-development pathway from identification and assay development to validation for clinical use.I recieved an honorarium from Roche Diagnostics for my participation in the advisory panel meeting leading to this pape

Advances in the therapy of Alzheimer's disease: Targeting amyloid beta and tau and perspectives for the future

Worldwide multidisciplinary translational research has led to a growing knowledge of the genetics and molecular pathogenesis of Alzheimer's disease (AD) indicating that pathophysiological brain alterations occur decades before clinical signs and symptoms of cognitive decline can be diagnosed. Consequently, therapeutic concepts and targets have been increasingly focused on early-stage illness before the onset of dementia; and distinct classes of compounds are now being tested in clinical trials. At present, there is a growing consensus that therapeutic progress in AD delaying disease progression would significantly decrease the expanding global burden. The evolving hypothesis- and evidence-based generation of new diagnostic research criteria for early-stage AD has positively impacted the development of clinical trial designs and the characterization of earlier and more specific target populations for trials in prodromal as well as in pre- and asymptomatic at-risk stages of AD