Fast STIR imaging of the heart with effective suppression of flow and motion artifacts was implemented. The approach has much potential for high-contrast imaging in a variety of diseases affecting the heart and mediastinum.

Objective-Myelination of the human brain results in roughly quadratic trajectories of myelin content and integrity, reaching a maximum in mid-life and then declining in older age. This trajectory is most evident in vulnerable later myelinating association regions such as frontal lobes and may be the biological substrate for similar trajectories of cognitive processing speed. Speed of movement, such as maximal finger tapping speed (FTS), requires high-frequency action potential (AP) bursts and is associated with myelin integrity. We tested the hypothesis that the age-related trajectory of FTS is related to brain myelin integrity.Methods-A sensitive in vivo MRI biomarker of myelin integrity (calculated transverse relaxation rates (R 2 )) of frontal lobe white matter (FLwm) was measured in a sample of very healthy males (N = 72) between 23 and 80 years of age. To assess specificity, R 2 of a contrasting early-myelinating region (splenium of the corpus callosum) was also measured.Results-FLwm R 2 and FTS measures were significantly correlated (r = .45, p < .0001) with no association noted in the early-myelinating region (splenium). Both FLwm R 2 and FTS had Conflict of interestThe authors have no actual or potential conflicts of interest.Disclosure statement All human subjects received written and oral information about the study and signed written informed consents approved by the local institutional review board prior to study participation. NIH Public Access NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript significantly quadratic lifespan trajectories that were virtually indistinguishable and both reached a peak at 39 years of age and declined with an accelerating trajectory thereafter. Conclusions-The results suggest that in this very healthy male sample, maximum motor speed requiring high-frequency AP burst may depend on brain myelin integrity. To the extent that the FLwm changes assessed by R 2 contribute to an age-related reduction in AP burst frequency, it is possible that other brain functions dependent on AP bursts may also be affected. Non-invasive measures of myelin integrity together with testing of basic measures of processing speed may aid in developing and targeting anti-aging treatments to mitigate age-related functional declines.

No abstract

Brain iron increases with age and is abnormally elevated early in the disease process in several neurodegenerative disorders that impact memory including Alzheimer's disease (AD). Higher brain iron levels are associated with male gender and presence of highly prevalent allelic variants in genes encoding for iron metabolism proteins (hemochromatosis H63D (HFE H63D) and transferrin C2 (TfC2)). In this study, we examined whether in healthy older individuals memory performance is associated with increased brain iron, and whether gender and gene variant carrier (IRON + ) vs noncarrier (IRONÀ) status (for HFE H63D/TfC2) modify the associations. Tissue iron deposited in ferritin molecules can be measured in vivo with magnetic resonance imaging utilizing the field-dependent relaxation rate increase (FDRI) method. FDRI was assessed in hippocampus, basal ganglia, and white matter, and IRON + vs IRONÀ status was determined in a cohort of 63 healthy older individuals. Three cognitive domains were assessed: verbal memory (delayed recall), working memory/attention, and processing speed. Independent of gene status, worse verbal-memory performance was associated with higher hippocampal iron in men (r ¼ À0.50, p ¼ 0.003) but not in women. Independent of gender, worse verbal working memory performance was associated with higher basal ganglia iron in IRONÀ group (r ¼ À0.49, p ¼ 0.005) but not in the IRON + group. Between-group interactions (p ¼ 0.006) were noted for both of these associations. No significant associations with white matter or processing speed were observed. The results suggest that in specific subgroups of healthy older individuals, higher accumulations of iron in vulnerable gray matter regions may adversely impact memory functions and could represent a risk factor for accelerated cognitive decline. Combining genetic and MRI biomarkers may provide opportunities to design primary prevention clinical trials that target high-risk groups.

T2-weighted breath-hold imaging, particularly IR-fast-SE imaging, was more sensitive for hepatic masses than conventional SE imaging, with a substantial reduction in acquisition time. Half-Fourier-single-shot-fast-SE imaging was especially useful in patients who were unable to hold their breath.

Prevalent gene variants involved in iron metabolism [hemochromatosis (HFE) H63D and transferrin C2 (TfC2)] have been associated with higher risk and earlier age at onset of Alzheimer’s disease (AD), especially in men. Brain iron increases with age, is higher in men, and is abnormally elevated in several neurodegenerative diseases, including AD and Parkinson’s disease, where it has been reported to contribute to younger age at onset in men. The effects of the common genetic variants (HFE H63D and/or TfC2) on brain iron were studied across eight brain regions (caudate, putamen, globus pallidus, thalamus, hippocampus, white matter of frontal lobe, genu, and splenium of corpus callosum) in 66 healthy adults (35 men, 31 women) aged 55 to 76. The iron content of ferritin molecules (ferritin iron) in the brain was measured with MRI utilizing the Field Dependent Relaxation Rate Increase (FDRI) method. 47% of the sample carried neither genetic variant (IRON−) and 53% carried one and/or the other (IRON+). IRON+ men had significantly higher FDRI compared to IRON− men (p = 0.013). This genotype effect was not observed in women who, as expected, had lower FDRI than men. This is the first published evidence that these highly prevalent genetic variants in iron metabolism genes can influence brain iron levels in men. Clinical phenomena such as differential gender-associated risks of developing neurodegenerative diseases and age at onset may be associated with interactions between iron genes and brain iron accumulation. Clarifying mechanisms of brain iron accumulation may help identify novel interventions for age-related neurodegenerative diseases.

We propose a simultaneous myocardial T1 and T2 mapping technique using a radial sequence with inversion recovery and T2 preparation, which achieves high accuracy and precision, with T1 and T2 reproducibility similar to the Modified Look‐Locker Inversion recovery (MOLLI) sequence and the conventional bright blood T2 mapping technique, respectively. The sequence was developed by incorporating gold angle radial fast low angle shot (FLASH) readout combined with an inversion pulse and T2prep pulses. The extended Bloch equation simulation with slice profile correction (BLESSPC) algorithm was proposed to reconstruct T1 and T2 maps at the same time in a few seconds, while maintaining good T1 and T2 estimation accuracy. Accuracy and precision were compared among the proposed technique, MOLLI and conventional T2 mapping techniques using phantom studies, 10 healthy volunteers and three patients. In phantom studies, the proposed technique was more accurate than MOLLI (P < 0.05) while achieving similar precision (P = 0.3) in T1 estimation, and was more accurate (P < 0.05) and precise (P < 0.001) than conventional T2 mapping (two‐parameter fitting) in T2 estimation. In vivo, the proposed technique achieved significantly higher T1 values (P < 0.001) and similar reproducibility (P = 0.3) compared with MOLLI, with significantly lower T2 values (P < 0.001) and similar reproducibility (P = 0.6) compared with the conventional T2 mapping technique. Thus, the proposed radial T1‐T2 mapping technique allows for accurate, precise, simultaneous myocardial T1 and T2 mapping in an 11‐heartbeat single breath‐hold acquisition.

Case reports tor delay, frontal bossing and temporal 'retraction', microcephaly, a large mouth with thin lips and downturned corners, a cleft or high arched palate, micrognathia, low set malformed ears, a short and/or webbed neck, a widow's peak, a low posterior hairline, widely spaced nipples, congenital heart defects, renal anomalies, rhizomelia, polydactyly, and hyperlaxity of limb joints. Several of these features were present in our case although her early death and lack of necropsy prevented further, more detailed examination being carried out. Interesting clinical findings in our case were the massive oedema, anaemia, and calcified gallstones. These features have not been described in any of the previous reports. It is possible that they may be the result of the deletion of the terminal region of 12p.