Anomalous hardness behaviour of high pressure die-cast mg-al alloys

The yield stress (0.2%) of 5 mm thick high pressure die-cast AZ91 and AM60 alloys has been compared to the respective Vickers hardness. The yield stress and hardness were measured in as-cast specimens, and in specimens directly aged (from the as-cast condition) at 120ºC for up to 10000 h. Unlike a range of sand cast and permanent mould cast Mg-Al alloys and an AZ91 alloy, for which the hardness increase proportionally to the yield stress, in high pressure die-cast magnesium alloys the hardness tends to be lower than expected from their yield stress

Author Correction: A HML6 endogenous retrovirus on chromosome 3 is upregulated in amyotrophic lateral sclerosis motor cortex

There is increasing evidence that endogenous retroviruses (ERVs) play a significant role in central nervous system diseases, including amyotrophic lateral sclerosis (ALS). Studies of ALS have consistently identified retroviral enzyme reverse transcriptase activity in patients. Evidence indicates that ERVs are the cause of reverse transcriptase activity in ALS, but it is currently unclear whether this is due to a specific ERV locus or a family of ERVs. We employed a combination of bioinformatic methods to identify whether specific ERVs or ERV families are associated with ALS. Using the largest post-mortem RNA-sequence datasets available we selectively identified ERVs that closely resembled full-length proviruses. In the discovery dataset there was one ERV locus (HML6_3p21.31c) that showed significant increased expression in post-mortem motor cortex tissue after multiple-testing correction. Using six replication post-mortem datasets we found HML6_3p21.31c was consistently upregulated in ALS in motor cortex and cerebellum tissue. In addition, HML6_3p21.31c showed significant co-expression with cytokine binding and genes involved in EBV, HTLV-1 and HIV type-1 infections. There were no significant differences in ERV family expression between ALS and controls. Our results support the hypothesis that specific ERV loci are involved in ALS pathology

A HML6 endogenous retrovirus on chromosome 3 is upregulated in amyotrophic lateral sclerosis motor cortex.

There is increasing evidence that endogenous retroviruses (ERVs) play a significant role in central nervous system diseases, including amyotrophic lateral sclerosis (ALS). Studies of ALS have consistently identified retroviral enzyme reverse transcriptase activity in patients. Evidence indicates that ERVs are the cause of reverse transcriptase activity in ALS, but it is currently unclear whether this is due to a specific ERV locus or a family of ERVs. We employed a combination of bioinformatic methods to identify whether specific ERVs or ERV families are associated with ALS. Using the largest post-mortem RNA-sequence datasets available we selectively identified ERVs that closely resembled full-length proviruses. In the discovery dataset there was one ERV locus (HML6_3p21.31c) that showed significant increased expression in post-mortem motor cortex tissue after multiple-testing correction. Using six replication post-mortem datasets we found HML6_3p21.31c was consistently upregulated in ALS in motor cortex and cerebellum tissue. In addition, HML6_3p21.31c showed significant co-expression with cytokine binding and genes involved in EBV, HTLV-1 and HIV type-1 infections. There were no significant differences in ERV family expression between ALS and controls. Our results support the hypothesis that specific ERV loci are involved in ALS pathology

The Sudbury Neutrino Observatory

The Sudbury Neutrino Observatory is a second generation water Cherenkov detector designed to determine whether the currently observed solar neutrino deficit is a result of neutrino oscillations. The detector is unique in its use of D2O as a detection medium, permitting it to make a solar model-independent test of the neutrino oscillation hypothesis by comparison of the charged- and neutral-current interaction rates. In this paper the physical properties, construction, and preliminary operation of the Sudbury Neutrino Observatory are described. Data and predicted operating parameters are provided whenever possible.Comment: 58 pages, 12 figures, submitted to Nucl. Inst. Meth. Uses elsart and epsf style files. For additional information about SNO see http://www.sno.phy.queensu.ca . This version has some new reference

Measurement of the νe and total 8B solar neutrino fluxes with the Sudbury Neutrino Observatory phase-III data set

This paper details the solar neutrino analysis of the 385.17-day phase-III data set acquired by the Sudbury Neutrino Observatory (SNO). An array of 3He proportional counters was installed in the heavy-water target to measure precisely the rate of neutrino-deuteron neutral-current interactions. This technique to determine the total active 8B solar neutrino flux was largely independent of the methods employed in previous phases. The total flux of active neutrinos was measured to be 5.54-0.31+0.33(stat.)-0.34+0.36(syst.)×106 cm-2 s-1, consistent with previous measurements and standard solar models. A global analysis of solar and reactor neutrino mixing parameters yielded the best-fit values of Δm2=7.59-0.21+0.19×10 -5eV2 and θ=34.4-1.2+1.3degrees

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

Suspeita de febre familiar dos cães Shar-peis chineses Suspected familiar chinese Shar-pei dog fever

A febre (síndrome) familiar dos cães Shar-peis Chineses é uma doença hereditária autossômica recessiva. Este trabalho descreve um caso de amiloidose generalizada em um cão Shar-pei Chinês, fêmea, de três anos de idade, cujo quadro clínico-patológico é consistente com o da febre familiar dos cães Shar-peis chineses. Esse animal tinha uma história clínica de edema bilateral recidivante na região do jarrete que vinha sendo observado desde os sete meses de idade. Três dias antes da morte, esse cão apresentou anorexia, apatia, vômito e diarréia. À necropsia, ambos os rins estavam firmes, pálidos e possuíam a superfície capsular irregular. Histologicamente foram observados depósitos de amilóide nos rins, no pâncreas, na tireóide e no baço. Esse amilóide perdeu sua afinidade para o vermelho Congo, quando utilizado o permanganato de potássio. Esse achado é consistente com amiloidose do tipo AA.<br>Chinese Shar-pei familial fever is a breed-associated hereditary autosomal recessive disease of Chinese Shar-pei dogs. A case of generalized amyloidosis in a 3-year-old female Chinese Shar-pei dog with a tentative diagnosis of familial Chinese Shar-pei fever is described. This animal had a clinical history of episodic bilateral swelling of the tarsal joints since 7-month-old. Vomiting, diarrhea, anorexia and lethargy were observed 3 days prior to death. At necropsy, both kidneys were firm, whitish and had an irregular capsular surface. Microscopically, amyloid deposits were observed in the kidneys, pancreas, thyroid glands and spleen. Amyloid deposits lost their affinity for Congo red after treatment with potassium permanganate indicating AA-type amyloidosis

Microstructure Formation in AlSi4MgMn and AlMg5Si2Mn High-Pressure Die Castings

Understanding microstructure formation during high-pressure die casting (HPDC) is important for the effective quality control of high-pressure diecast aluminum-alloy components for high-integrity applications. In this study, two HPDC-specific aluminum alloys, AlSi4MgMn and AlMg5Si2Mn, were cast into tensile test bars by cold-chamber (CC) HPDC. The microstructures of the tensile bar specimens were characterized at different length scales, from the scale of the casting to the scale of the eutectic interlamellar spacing. The results show that the salient as-cast microstructural features, e.g., externally solidified crystals (ESCs), defect bands, the surface layer, grain size distribution, porosity, and hot tears were similar for both alloys. The formation of these features can be understood by considering the influence of flow and solidification during each stage of the HPDC process

Necropsy diagnosis of myocarditis: a retrospective study using CD45RO immunohistochemistry

Aim—To use CD45RO immunohistochemistry to investigate the numbers of T lymphocytes found in sections of myocardium from a routine necropsy series, and to determine the incidence of myocarditis in this series. Methods—Myocardial sections from 163 routine hospital necropsies were stained with CD45RO and the numbers of positive lymphocytes/mm(2) were counted. The results were correlated with the H/E opinion and the clinical context of the necropsy. Results—Most (143) cases showed low numbers (0–3) of CD45RO positive lymphocytes/mm(2). Fifteen cases showed 7–13 positive lymphocytes/mm(2), comprising a wide variety of clinical conditions, generally with no specific cardiac pathology. Five cases showed 14 or more positive lymphocytes/mm(2), comprising one case of active myocarditis, three cases of cardiac transplant rejection, and one post-transplant lymphoproliferative disorder, all conditions in which large numbers of lymphocytes would be expected. Conclusions—The incidence of myocarditis in our series was 0.6%. In most cases the normal myocardium has a low T lymphocyte count (0–3/mm(2)). In some cases immunohistochemistry shows more positive cells than would have been expected on light microscopy. Immunohistochemistry is a useful and reliable means of confirming a diagnosis of myocarditis. The results support the conclusion of the 1997 ISFC task force that 14 or more lymphocytes or macrophages/mm(2) of myocardium in the appropriate clinical context is a reliable threshold for the diagnosis of chronic myocarditis. Key Words: myocarditis • immunohistochemistry • T lymphocytes • necrops