Sleep slow oscillations favour local cortical plasticity underlying the consolidation of reinforced procedural learning in human sleep

We investigated changes of slow‐wave activity and sleep slow oscillations in the night following procedural learning boosted by reinforcement learning, and how these changes correlate with behavioural output. In the Task session, participants had to reach a visual target adapting cursor's movements to compensate an angular deviation introduced experimentally, while in the Control session no deviation was applied. The task was repeated at 13:00 hours, 17:00 hours and 23:00 hours before sleep, and at 08:00 hours after sleep. The deviation angle was set at 15° (13:00 hours and 17:00 hours) and increased to 45° (reinforcement) at 23:00 hours and 08:00 hours. Both for Task and Control nights, high‐density electroencephalogram sleep recordings were carried out (23:30?19:30 hours). The Task night as compared with the Control night showed increases of: (a) slow‐wave activity (absolute power) over the whole scalp; (b) slow‐wave activity (relative power) in left centro‐parietal areas; (c) sleep slow oscillations rate in sensorimotor and premotor areas; (d) amplitude of pre‐down and up states in premotor regions, left sensorimotor and right parietal regions; (e) sigma crowning the up state in right parietal regions. After Task night, we found an improvement of task performance showing correlations with sleep slow oscillations rate in right premotor, sensorimotor and parietal regions. These findings suggest a key role of sleep slow oscillations in procedural memories consolidation. The diverse components of sleep slow oscillations selectively reflect the network activations related to the reinforced learning of a procedural visuomotor task. Indeed, areas specifically involved in the task stand out as those with a significant association between sleep slow oscillations rate and overnight improvement in task performance.     

Neurochemical correlates of caudate atrophy in Huntington's disease

The precise pathogenic mechanisms of Huntington's disease (HD) are unknown but can be tested in vivo using proton magnetic resonance spectroscopy (¹H MRS) to measure neurochemical changes. The objective of this study was to evaluate neurochemical differences in HD gene mutation carriers (HGMCs) versus controls and to investigate relationships among function, brain structure, and neurochemistry in HD. Because previous ¹H MRS studies have yielded varied conclusions about HD neurochemical changes, an additional goal was to compare two ¹H MRS data analysis approaches. HGMCs with premanifest to early HD and controls underwent evaluation of motor function, magnetic resonance imaging, and localized ¹H MRS in the caudate and the frontal lobe. Analytical approaches that were tested included absolute quantitation (unsuppressed water signal as an internal reference) and relative quantification (calculating ratios of all neurochemical signals within a voxel). We identified a suite of neurochemicals that were reduced in concentration proportionally to loss of caudate volume in HGMCs. Caudate concentrations of N‐acetylaspartate (NAA), creatine, choline, and caudate and frontal lobe concentrations of glutamate plus glutamine (Glx) and glutamate were correlated with caudate volume in HGMCs. The relative, but not the absolute, quantitation approach revealed disease‐related differences; the Glx signal was decreased relative to other neurochemicals in the caudate of HGMCs versus controls. This is the first study to demonstrate a correlation among structure, function, and chemical measures in HD brain. Additionally, we demonstrate that a relative quantitation approach may enable the magnification of subtle differences between groups. Observation of decreased Glx suggests that glutamate signaling may be disrupted relatively early in HD, which has important implications for therapeutic approaches. © 2014 International Parkinson and Movement Disorder Society     

Molecular Epidemiology of Hospital Outbreak of Middle East Respiratory Syndrome,Riyadh, Saudi Arabia, 2014

We investigated an outbreak of Middle East respiratory syndrome (MERS) at King Fahad Medical City (KFMC), Riyadh, Saudi Arabia, during March 29–May 21, 2014. This outbreak involved 45 patients: 8 infected outside KFMC, 13 long-term patients at KFMC, 23 health care workers, and 1 who had an indeterminate source of infection. Sequences of full-length MERS coronavirus (MERS-CoV) from 10 patients and a partial sequence of MERS-CoV from another patient, when compared with other MERS-CoV sequences, demonstrated that this outbreak was part of a larger outbreak that affected multiple health care facilities in Riyadh and possibly arose from a single zoonotic transmission event that occurred in December 2013 (95% highest posterior density interval November 8, 2013–February 10, 2014). This finding suggested continued health care–associated transmission for 5 months. Molecular epidemiology documented multiple external introductions in a seemingly contiguous outbreak and helped support or refute transmission pathways suspected through epidemiologic investigation.     

Monosomy of chromosome 17 in breast cancer during interpretation of HER2 gene amplification

Monosomy of chromosome 17 may affect the assessment of HER2 amplification. Notably, the prevalence ranges from 1% up to 49% due to lack of consensus in recognition. We sought to investigate the impact of monosomy of chromosome 17 to interpretation of HER2 gene status. 201 breast carcinoma were reviewed for HER2 gene amplification and chromosome 17 status. FISH analysis was performed by using double probes (LSI/CEP). Absolute gene copy number was also scored per each probe. HER2 FISH test was repeated on serial tissue sections, ranging in thickness from 3 to 20 µm. Ratio was scored and subsequently corrected by monosomy after gold control test using the aCGH method to overcome false interpretation due to artefactual nuclear truncation. HER2 immunotests was performed on all cases. 26/201 cases were amplified (13%). Single signals per CEP17 were revealed in 7/201 (3.5%) cases. Five out of 7 cases appeared monosomic with aCGH (overall, 5/201, 2.5%) and evidenced single signals in >60% of nuclei after second-look on FISH when matching both techniques. Among 5, one case showed amplification with a pattern 7/1 (HER2/CEP17>2) of copies (3+ at immunotest); three cases revealed single signals per both probes (LSI/CEP=1) and one case revealed a 3:1 ratio; all last 4 cases showed 0/1+ immunoscore. We concluded that: 1) monosomy of chromosome 17 may be observed in 2.5% of breast carcinoma; 2) monosomy of chromosome 17 due to biological reasons rather than nuclear truncation was observed when using the cut-off of 60% of nuclei harboring single signals; 3) the skewing of the ratio due to single centromeric 17 probe may lead to false positive evaluation; 4) breast carcinomas showing a 3:1 ratio (HER2/CEP17) usually show negative 0/1+ immunoscore and <6 gene copy number at FISH.     

A high-titer,high-thermal-amplitude autoanti-B associated with acrocyanosis but no obvious hemolytic anemia

BACKGROUND: ABO autoantibodies are rare. Most reported examples have been antibodies with 4 degrees C titers not greater than 256 in patients without apparent hemolytic anemia. Most high-titer, high-thermal-amplitude, complement-activating cold agglutinins are associated with hemolytic anemia. STUDY DESIGN AND METHODS: A 52-year-old man presented with acrocyanosis and mild small-vessel brain disease, but no evidence of obvious hemolytic anemia. Regular plasmapheresis treatment was helpful in relieving the clinical symptoms associated with acrocyanosis. Serologic methods were used to study the patient's RBCs and sera. RESULTS: The patient's RBCs were strongly reactive with anti-C3 and anti-IgM and weakly reactive with anti-IgA. The patient's serum contained a high-titer, high-thermal-amplitude, IgMkappa autoanti-B, capable of activating complement in vitro. CONCLUSION: A patient with a powerful ABO autoantibody is described. This patient had acrocyanosis but did not appear to have an obvious hemolytic anemia. This case is a good example of the lack of correlation between in vitro serologic tests and in vivo reactions in individual patients.     

Cannon‐ball bladder stones: a complication of prolonged recumbence and benign prostate enlargement

Chronically bedridden patients are predisposed to various urological complications such as urinary infections, incomplete urinary bladder emptying after voiding and stone formation in the urinary tract, more so in the absence of good nursing care. Multiple giant bladder stones giving rise to ‘cannon ball’ appearance have rarely been reported. We present the case of an 85‐year‐old frail gentleman who was bedridden for the last 25 years and presented with haematuria. On evaluation he was found to have multiple large bladder stones and bladder diverticuli with enlarged prostate gland. This case highlights a relatively rare urological complication of prolonged recumbency, and emphasizes the importance of proper nursing care, early detection, management and prevention of such complications.