(Benzonitrile-κN)chlorido[hydrido­tris(pyrazol-1-yl-κN 2)borato](triphenyl­phosphine-κP)ruthenium(II) ethanol solvate. Corrigendum

Corrigendum to Acta Cryst. (2009), E65, m438

(Benzonitrile-κN)chlorido[hydrido­tris(pyrazol-1-yl-κN 2)borato](triphenyl­phosphine-κP)ruthenium(II) ethanol solvate

The reaction of [Ru(C9H10BN6)Cl(C18H15P)2] with benzo­nitrile leads to crystals of the title compound, [Ru(C9H10BN6)Cl(C18H15P)(C7H5N)]·C2H5OH. In the crystal structure, the environment about the ruthenium metal center corresponds to a slightly distorted octa­hedron with an average N—Ru—N bite angle of the Tp ligand of 86.6 (2)°

Aberrant Sensory Gating of the Primary Somatosensory Cortex Contributes to the Motor Circuit Dysfunction in Paroxysmal Kinesigenic Dyskinesia

Paroxysmal kinesigenic dyskinesia (PKD) is conventionally regarded as a movement disorder (MD) and characterized by episodic hyperkinesia by sudden movements. However, patients of PKD often have sensory aura and respond excellently to antiepileptic agents. PRRT2 mutations, the most common genetic etiology of PKD, could cause epilepsy syndromes as well. Standing in the twilight zone between MDs and epilepsy, the pathogenesis of PKD is unclear. Gamma oscillations arise from the inhibitory interneurons which are crucial in the thalamocortical circuits. The role of synchronized gamma oscillations in sensory gating is an important mechanism of automatic cortical inhibition. The patterns of gamma oscillations have been used to characterize neurophysiological features of many neurological diseases, including epilepsy and MDs. This study was aimed to investigate the features of gamma synchronizations in PKD. In the paired-pulse electrical-stimulation task, we recorded the magnetoencephalographic data with distributed source modeling and time-frequency analysis in 19 patients of newly-diagnosed PKD without receiving pharmacotherapy and 18 healthy controls. In combination with the magnetic resonance imaging, the source of gamma oscillations was localized in the primary somatosensory cortex. Somatosensory evoked fields of PKD patients had a reduced peak frequency (p < 0.001 for the first and the second response) and a prolonged peak latency (the first response p = 0.02, the second response p = 0.002), indicating the synchronization of gamma oscillation is significantly attenuated. The power ratio between two responses was much higher in the PKD group (p = 0.013), indicating the incompetence of activity suppression. Aberrant gamma synchronizations revealed the defective sensory gating of the somatosensory area contributes the pathogenesis of PKD. Our findings documented disinhibited cortical function is a pathomechanism common to PKD and epilepsy, thus rationalized the clinical overlaps of these two diseases and the therapeutic effect of antiepileptic agents for PKD. There is a greater reduction of the peak gamma frequency in PRRT2-related PKD than the non-PRRT PKD group (p = 0.028 for the first response, p = 0.004 for the second response). Loss-of-function PRRT2 mutations could lead to synaptic dysfunction. The disinhibiton change on neurophysiology reflected the impacts of PRRT2 mutations on human neurophysiology

Pan-cancer analysis of whole genomes

Cancer is driven by genetic change, and the advent of massively parallel sequencing has enabled systematic documentation of this variation at the whole-genome scale(1-3). Here we report the integrative analysis of 2,658 whole-cancer genomes and their matching normal tissues across 38 tumour types from the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA). We describe the generation of the PCAWG resource, facilitated by international data sharing using compute clouds. On average, cancer genomes contained 4-5 driver mutations when combining coding and non-coding genomic elements; however, in around 5% of cases no drivers were identified, suggesting that cancer driver discovery is not yet complete. Chromothripsis, in which many clustered structural variants arise in a single catastrophic event, is frequently an early event in tumour evolution; in acral melanoma, for example, these events precede most somatic point mutations and affect several cancer-associated genes simultaneously. Cancers with abnormal telomere maintenance often originate from tissues with low replicative activity and show several mechanisms of preventing telomere attrition to critical levels. Common and rare germline variants affect patterns of somatic mutation, including point mutations, structural variants and somatic retrotransposition. A collection of papers from the PCAWG Consortium describes non-coding mutations that drive cancer beyond those in the TERT promoter(4); identifies new signatures of mutational processes that cause base substitutions, small insertions and deletions and structural variation(5,6); analyses timings and patterns of tumour evolution(7); describes the diverse transcriptional consequences of somatic mutation on splicing, expression levels, fusion genes and promoter activity(8,9); and evaluates a range of more-specialized features of cancer genomes(8,10-18).Peer reviewe

Welded microstructure and orientation variation of duplex Ti alloy through electrodynamic vibration

Duplex Ti alloys are widely used in the petrochemical industry as well as in the biomedical, aeronautics and astronautics engineering fields. A duplex Ti alloy weldment is uniform and has superior properties in terms of welded microstructure evolution, grain refinement, and microhardness distribution. These properties are believed to be obtainable through tungsten inert gas arc welding with a combination of electrodynamic vibration and active flux. This combination changes the welded metal to phase transformation products, leading to the reappearance of numerous low-angle grain boundaries (≤5°). Vibration is presumed to disturb the heat transfer and temperature gradient in a liquid melt welding pool, enhancing the nucleation and cooling rates. The final result is the rapid formation of many basket weave-like fine parallel elongated α′ sheaths containing the β-phase in the solidified welded metal

Clinical Application of Metagenomic Next-Generation Sequencing in Patients with Hematologic Malignancies Suffering from Sepsis

Background: Sepsis remains a common but fatal complication among patients with immune suppression. We aimed to investigate the performance of metagenomic next-generation sequencing (mNGS) compared with standard microbiological diagnostics in patients with hematologic malignancies. Methods: We performed a prospective study from June 2019 to December 2019. Adult patients with hematologic malignancies and a clinical diagnosis of sepsis were enrolled. Conventional diagnostic methods included blood cultures, serum galactomannan for Aspergillus, cryptococcal antigen and cytomegalovirus (CMV) viral loads. Blood samples for mNGS were collected within 24 h after hypotension developed. Results: Of 24 patients enrolled, mNGS and conventional diagnostic methods (blood cultures, serology testing and virus RT-PCR) reached comparable positive results in 9 cases. Of ten patients, mNGS was able to identify additional pathogens compared with conventional methods; most of the pathogens were virus. Conclusion: Our results show that mNGS may serve as adjunctive diagnostic tool for the identification of pathogens of hematologic patients with clinically sepsis

Clinical Application of Metagenomic Next-Generation Sequencing in Patients with Hematologic Malignancies Suffering from Sepsis

Background: Sepsis remains a common but fatal complication among patients with immune suppression. We aimed to investigate the performance of metagenomic next-generation sequencing (mNGS) compared with standard microbiological diagnostics in patients with hematologic malignancies. Methods: We performed a prospective study from June 2019 to December 2019. Adult patients with hematologic malignancies and a clinical diagnosis of sepsis were enrolled. Conventional diagnostic methods included blood cultures, serum galactomannan for Aspergillus, cryptococcal antigen and cytomegalovirus (CMV) viral loads. Blood samples for mNGS were collected within 24 h after hypotension developed. Results: Of 24 patients enrolled, mNGS and conventional diagnostic methods (blood cultures, serology testing and virus RT-PCR) reached comparable positive results in 9 cases. Of ten patients, mNGS was able to identify additional pathogens compared with conventional methods; most of the pathogens were virus. Conclusion: Our results show that mNGS may serve as adjunctive diagnostic tool for the identification of pathogens of hematologic patients with clinically sepsis

Effect of Natural Ageing on Subsequent Artificial Ageing of AA7075 Aluminum Alloy

The effects of natural ageing treatment prior to artificial ageing treatment on the microstructures and mechanical properties of AA7075 Al-5.7Zn-2.6Mg-1.5Cu-0.18Cr-0.08Mn-0.05Si-0.17Fe (wt.%) aluminum alloy have been investigated. The hardness of solution-treated samples (91.0 HV) profoundly increased to 146.8 HV after 7 days of natural ageing. The purpose of the present work was to examine the kinetic hardening evolution in subsequent artificial ageing treatments of samples naturally aged for 7 days and their counterparts without natural ageing. The former were labelled as NA-7d samples, and the latter, NA-0d samples. After artificial ageing at 120 °C for 2 h, the hardness of NA-0d samples increased rapidly to 148.2 HV, which was approximately the same as that of the specimens with natural ageing for 7 days, compensating for the prior state of lower hardness without natural ageing. After being treated at 120 °C for 16 h, the ultimate tensile strength (UTS) and yield strength (YS) of NA-7d reached the highest value, respectively, 601 MPa and 539 MPa, followed by a slight decrement of UTS when aged to 24 h. On the other hand, NA-0d specimens aged at 120 °C for 16 and 24 h showed nearly the same UTS (598 MPa); the former possessed YS of 538 MPa, and the latter, 545 MPa. The results presumably reveal that the peak ageing condition for NA-0d samples can be achieved under 24 h ageing at 120 °C. Under the same treatment at 120 °C for 24 h, the size of η’ phase in NA-7d sample (with a length of 4.96 nm) coarsened and grew larger than that in NA-0d sample (with a length of 3.46 nm). In addition, some η’ phase in the NA-7d sample was found to be transformed into the η2 phase. The results indicated that the naturally aged specimens (NA-7d) reached the peak ageing condition earlier, but did not significantly enhance the UTS in AA7075 aluminum alloy, as compared to the samples without prior natural ageing (NA-0d)

Effect of Natural Ageing on Subsequent Artificial Ageing of AA7075 Aluminum Alloy

The effects of natural ageing treatment prior to artificial ageing treatment on the microstructures and mechanical properties of AA7075 Al-5.7Zn-2.6Mg-1.5Cu-0.18Cr-0.08Mn-0.05Si-0.17Fe (wt.%) aluminum alloy have been investigated. The hardness of solution-treated samples (91.0 HV) profoundly increased to 146.8 HV after 7 days of natural ageing. The purpose of the present work was to examine the kinetic hardening evolution in subsequent artificial ageing treatments of samples naturally aged for 7 days and their counterparts without natural ageing. The former were labelled as NA-7d samples, and the latter, NA-0d samples. After artificial ageing at 120 °C for 2 h, the hardness of NA-0d samples increased rapidly to 148.2 HV, which was approximately the same as that of the specimens with natural ageing for 7 days, compensating for the prior state of lower hardness without natural ageing. After being treated at 120 °C for 16 h, the ultimate tensile strength (UTS) and yield strength (YS) of NA-7d reached the highest value, respectively, 601 MPa and 539 MPa, followed by a slight decrement of UTS when aged to 24 h. On the other hand, NA-0d specimens aged at 120 °C for 16 and 24 h showed nearly the same UTS (598 MPa); the former possessed YS of 538 MPa, and the latter, 545 MPa. The results presumably reveal that the peak ageing condition for NA-0d samples can be achieved under 24 h ageing at 120 °C. Under the same treatment at 120 °C for 24 h, the size of η’ phase in NA-7d sample (with a length of 4.96 nm) coarsened and grew larger than that in NA-0d sample (with a length of 3.46 nm). In addition, some η’ phase in the NA-7d sample was found to be transformed into the η2 phase. The results indicated that the naturally aged specimens (NA-7d) reached the peak ageing condition earlier, but did not significantly enhance the UTS in AA7075 aluminum alloy, as compared to the samples without prior natural ageing (NA-0d)

Gastroesophageal Reflux Disease and Sleep Quality in a Chinese Population

Although evidence suggests that gastroesophageal reflux disease (GERD) may interrupt sleep, the effects of symptomatic and endoscopically diagnosed GERD remain elusive because the patient population is heterogeneous. Accordingly, we designed a cross-sectional study to assess their association. Methods: Consecutive participants in a routine health examination were enrolled. Definition and severity of erosive esophagitis were assessed using the Los Angeles classification system. Demographic data, reflux symptoms, sleep quality and duration, exercise amount, alcohol consumption, and smoking habits were recorded. Factors affecting sleep quality and sleep duration were revealed by a polytomous logistic regression analysis. Results: A total of 3663 participants were recruited. Subjects with reflux symptoms, female gender, higher body mass index, and regular use of hypnotics had poorer sleep quality. Exercise was associated with better sleep quality. Either symptomatically or endoscopically, GERD did not disturb sleep duration. Among the 3158 asymptomatic patients, those with erosive esophagitis were more likely to have poor sleep quality. The risk increased with the severity of erosive changes (p = 0.03). Conclusion: The present study highlights the adverse effect of gastroesophageal reflux on sleep, even in the absence of reflux symptoms. This finding has therapeutic implications in patients with silent erosive disease, and future trials are warranted